Emerging and Re-emerging

D i s e a s e s o f S e l e c t e d Avi a n
S p ec ie s
Anthony A. Pilny, DVM, DABVP (Avian Practice)a,*,
Drury Reavill, DVM, DABVP (Avian and Reptile/Amphibian Practice), DACVPb

KEYWORDS
 Emerging disease  Re-emerging disease  Avian  Infection  Welfare

KEY POINTS
 The identification of emerging and re-emerging diseases of birds relates not only to scien-
tific discovery, research, and species survival—but holds significant human health impli-
cations also.
 Emerging infections can be caused by numerous factors, including previously unknown
infectious agents, previously known agents whose role in specific diseases has been un-
recognized, and re-emergence of agents whose incidence of disease had declined or dis-
appeared in the past and whose incidence has reappeared.
 Emerging and re-emerging diseases can have impacts on avian welfare, livestock produc-
tion, and entire ecosystem health, and their recognition is of critical importance.

INTRODUCTION

The identification and significance of emerging and re-emerging diseases of birds re-
lates not only to scientific discovery and research, but holds significant human health
implications also. Two examples are bromethalin rodenticide toxicosis in wild birds
living in urban areas and the worldwide disease of cercarial dermatitis (swimmer’s
itch). Diseases may be zoonotic or have farm production implications, present as large
die-offs, and can affect zoo collections. Often, identification comes after large losses
are seen and some require elimination of hosts, such as infection with exotic Newcas-
tle disease in the poultry industry. Others can affect wild populations and affect
smaller ecosystems when large die-offs are seen. Also, bird migration provides a
mechanism for the establishment of new endemic disease at distances from where
an infection was initially acquired.
Emerging diseases can be caused by numerous factors, including previously unde-
tected or unknown infectious agents, known agents that have spread to new

a
Arizona Exotic Animal Hospital, 20040 N 19th Avenue Suite C, Phoenix, AZ 85027, USA;
b
ZNLabs, 525 E 4500 South Suite F200, Salt Lake City, UT 84107, USA
* Corresponding author.
E-mail address: apilny@azeah.com

Vet Clin Exot Anim 23 (2020) 429–441

https://doi.org/10.1016/j.cvex.2020.01.013 vetexotic.theclinics.com
1094-9194/20/ª 2020 Elsevier Inc. All rights reserved.
430 Pilny & Reavill

geographic locations or populations, and previously known agents whose role in spe-
cific diseases had previously been unrecognized. Agents whose incidence of disease
had declined or disappeared in the past, but whose incidence has reappeared are
known as re-emerging infectious diseases. The identification and our understanding
of these diseases remains critical.
This article summarizes selected emerging and re-emerging diseases of selected
avian species and complements other avian articles in this issue. Many more diseases
exist than the scope of this article allows, and many more currently remain
undiscovered.

Bromethalin Toxicity
Bromethalin is an odorless lipid soluble chemical, used as a rodenticide since the
1980s and designed to kill with a single ingestion. It is rapidly absorbed from the diges-
tive tract and once demethylated to its more potent metabolite, desmethyl-
bromethalin it readily crosses the blood-brain barrier. It acts by uncoupling oxidative
phosphorylation resulting in decreased adenosine triphosphate (ATP).1,2 A decline in
ATP leads to intracellular accumulation of sodium and an influx of water (cytotoxic
edema) and splitting of myelin sheaths (intramyelinic edema).2–5 The salient histologic
feature is of vacuolar degeneration primarily of cerebellar white matter (Fig. 1). There is
no specific antidote for the toxin.
Susceptibility to bromethalin varies by species, with domestic cats (Felis catus
domestica) being particularly susceptible, whereas guinea pigs (Cavia porcellus) are
considered resistant. In 1 tested avian species, adult Quail (Coturnix coturnix), the me-
dium oral lethal dose is similar to domestic mice and domestic dogs. Acute toxicosis in
domestic dogs and cats present with hyperexcitability, seizures, diffuse fine tremors,
pelvic limb ataxia and weakness, anisocoria, blindness, abnormal nystagmus, coma,
and death from respiratory arrest.2–5 Seizures tend to occur in the later stages of intox-
ication and are more commonly seen in cats than dogs. Chronic toxicosis appears
similar to acute with a delay in the development of the clinical signs. It is possible
that these domestic species could survive with subacute or chronic exposure.3,5

Fig. 1. Conure (Aratinga species). The prominent and consistent lesion of bromethalin toxi-
cosis is of cerebellar white matter vacuolization (asterisk) with increased cellularity due to
gliosis (hematoxylin-eosin stain). (Courtesy of D. R. Reavill, DVM, DABVP (Avian and Reptile
& Amphibian Practice), DACVP, Salt Lake City, UT.)
 Re-emerging Diseases of Selected Avian Species 431

The public noticed birds with neurologic clinical signs in a feral conure population in
San Francisco monitored since the 1990s. In 2003, these birds were brought to Mick-
aboo Companion Bird Rescue, which arranged for veterinary care at area hospitals. A
concerted effort was made in 2013 to determine a cause for the symptoms in these
birds with chronic neurologic signs that seldom resolved even with aggressive sup-
portive care. Based on clinical signs, histologic lesions in the brain, and positive tests
for desmethyl-bromethalin in the feces, and brain and liver tissues, it has been deter-
mined that these birds were suffering chronic bromethalin toxicity. A definitive source
has not been identified.6
The birds develop paresis, circling, ataxia, and seizures that are progressive until they
are unable to feed themselves. The differential diagnosis based on the clinical signs in-
cludes aberrant migration of Baylisascaris, protozoal infections, such as sarcocystis,
and less likely toxoplasma, paramyxoviruses, West Nile virus, avian bornavirus, lead
toxicity, and trauma.6 Positive testing for bromethalin was found in all examined birds.
There has been at least 1 incidence where bromethalin toxicity was suspected in
bald eagles (Haliaeetus leucocephalus) and American coots (Fulica americana). The
eagles were observed overflying perches or colliding with rock walls. Limb paresis
and incoordination were observed in American coots. Increased mortality occurred
over 2 winters in Arkansas. The consistent histologic finding was of the spongy degen-
eration of the white matter of the central nervous system.7
Antemortem testing is possible by bromethalin quantification in fecal samples in
acute cases. Postmortem testing requires frozen tissue samples of brain and liver
and seems to be diagnostic in chronic cases. Treatment of bromethalin toxicity is
based on decontamination (emesis and activated charcoal) if possible, control of cen-
tral nervous system signs, and supportive care.

Virulent Newcastle Disease

Virulent Newcastle disease is one of the most serious reportable poultry diseases
worldwide.8 Until this re-emergence, the US poultry industry was considered
disease-free since the last outbreak in 2002 to 2003, the only exception being some
species of wild birds implicated as reservoirs. Formerly known as exotic Newcastle
disease, this is a contagious and fatal viral disease affecting the respiratory, nervous,
and digestive systems of birds. The disease is so virulent that many birds die without
showing any clinical signs. A death rate of almost 100% can occur in unvaccinated
poultry flocks; moreover, it can infect and cause death even in vaccinated poultry.
Virulent Newcastle disease spreads when healthy birds come in direct contact with
bodily fluids from sick birds. In addition, the virus can travel on manure, egg flats,
crates, other farming materials or equipment, and people who have picked up the virus
on their hands or clothing. It has been shown to replicate in the reproductive tract of
adult hens.9
Clinical signs in chickens include:
 Sudden death and increased death loss in flocks
 Respiratory symptoms, including sneezing, gasping for air, nasal discharge, and
coughing
 Greenish, watery diarrhea, lethargy, tremors, and drooped wings
 Torticollis, circling, complete stiffness, and swelling around the eyes and neck
Understanding the potential risks of transmission of chicken- and wild bird-origin
virulent Newcastle disease in poultry is critical in outbreak response and control. Inad-
equate biosecurity measures poses a risk to the poultry industry of a Newcastle
disease-free country, with the possibility of transmission due to contacts at the
432 Pilny & Reavill

wildlife-poultry interface.10 Suspected cases should be tested or verified with nec-

ropsy and reported to the respective state veterinarian or the United States Depart-
ment of Agriculture (USDA).
As of October 2019 the USDA has confirmed 451 premises as infected in California
and 1 premises each in Utah and Arizona. This disease is not a food safety concern but
more so of biosecurity for the poultry industry.

Sarcocystis calchasi
The apicomplexan parasite Sarcocystis calchasi has been identified as the causative
agent of pigeon protozoal encephalitis (PPE), an emerging, severe neurologic disease
in domestic pigeons (Columba livia f. domestica).11,12 Pigeons serve as intermediate
hosts in the lifecycle of S calchasi, and the European subspecies of the Northern
goshawk (Accipiter g. gentilis) and the European sparrowhawk (Accipiter nisus)
have so far been identified as definitive hosts.13
Also, several psittacine species, including princess parrots and cockatoos, have
been reported as susceptible intermediate host species to natural infections.14 Clinical
signs and pathologic lesions in these psittacines closely resemble PPE and include
central nervous system signs of torticollis, nystagmus, ataxia, inability to stand, and
star-gazing. Experimental infection in cockatiels showed development of disease
similar to PPE also, and suggests possible ongoing dissemination of the parasite.15
Pigeons infected with S calchasi show a biphasic disease initially with polyuria, diar-
rhea, and lethargy. In the later periods of infection, central nervous signs, such as torti-
collis and opisthotonos associated with severe brain lesions, have been observed.
Mature tissue cysts can be observed in skeletal muscles in the postinfection stage
and the encephalitis is associated with the schizont stage of the parasite’s develop-
ment (Fig. 2). A recent report described acute death in 4 Roller pigeons naturally
infected at a zoo that had schizonts and free merozoites in the liver and spleen without
lesions or protozoa in the brain and muscles.16 Histologic and molecular characteriza-
tion of this disease are described in white winged and Eurasian collared doves.17 All
these reports suggest the disease has been found in wide-ranging areas and it is likely
the parasite has been present for some time and only recently described and
recognized.

Baylisascaris procyonis
The nematodes of Baylisascaris species are well recognized as causes of cerebrospi-
nal nematodiasis of North American animals. Baylisascaris procyonis is the most com-
mon cause of visceral, ocular larva migrans (OLM), and neural larva migrans (NLM),

Fig. 2. An intramyocytic thin-walled sarcocyst filled with numerous bradyzoites in skeletal

muscle of a dove.
 Re-emerging Diseases of Selected Avian Species 433

using the raccoon (Procyon lotor) as the primary host. There are 2 other Baylisascaris
species that have been infrequently incriminated; Baylisascaris columnaris that cycles
through skunks, and B melis of badgers. These nematode parasites have less ten-
dency to result in OLM and NLM.18 Over 130 species of mammals and birds, as
well as man, can serve as paratenic hosts.18,19 This indicates that the parasite is
highly nonspecific for paratenic hosts. Larva migrans from B procyonis has also
been reported in Europe and Japan where raccoons have been imported as part of
zoo collections and/or have become part of the wildlife fauna.20
These large ascarid nematodes mature in the intestines of the host. Infected rac-
coons can shed millions of parasitic eggs per day. These will typically accumulate
within communal defecation sites, which are described as latrines. The shed eggs
from the primary host can survive for extended periods within the environment as
well as within contaminated cages and enclosures. Birds and small mammals serve
as paratenic (transport) hosts. They are infected when they ingest the eggs from
contaminated environments. These eggs hatch and larval nematodes will aggressively
migrate through the tissues of the paratenic hosts, commonly resulting in neurologic
damage. It takes very few migrating larvae to result in a fatal central nervous system
disease.20 The life cycle is completed when raccoons eat infected animals with the
larvae either within the central nervous system or encapsulated in visceral tissues.18
In avian species, there have been many outbreaks within ranching situations, such
as with pheasants, emus, ostriches, bobwhites, and chucker partridges.21–24 A variety
of zoo birds have also succumbed to NLM when coming in contact with raccoon
latrines.25 Some pet bird species have been exposed by contact to contaminated
environment and/or transport containers. These have included cockatoos, macaws,
Patagonian conures, and cockatiels.26,27
The clinical signs are typical for central nervous system infections: loss of equilib-
rium, increasing ataxia, circling, torticollis, head tilts, visual defects, and being unable
to stand or walk. There may be grossly noticeable malacia and hemorrhage in the
brains, although absent to minimal lesions are more common. Histologically there
will be a nonsuppurative inflammatory reaction with gliosis and perivascular prolifera-
tions of lymphocytes and plasma cells. In some cases, the migration tracks can be
identified. Although this is a large nematode larva, these can be very difficult to identify
within sections of the brain (Fig. 3). In histologic sections, the third-stage larvae of
Baylisascaris species are all similar, so species determination in cases is near impos-
sible without epidemiologic study27–29 or molecular diagnostics. In general, it is very
uncommon to see visceral lesions of the larval migrations in birds. It has been sus-
pected in some cases where there have been granulomas identified in the heart, liver,
and kidney.19,26 Experimentally in chickens extraneural lesions were limited to focal
choroiditis and a larval granuloma in an extrinsic ocular muscle.30
If there are identified cases of Baylisascaris encephalitis, it is important to clean the
environment. This includes identifying where there are raccoon latrines. Removal of
contaminated soil or contaminated bedding material is necessary. It is also important
that any cages that have housed raccoons as well as skunks and badgers should be
thoroughly and fastidiously cleaned to remove any fecal material that may be support-
ing the nematode eggs.

Schistosomes
Schistosomes belong to a large family of trematodes that use snails as the intermedi-
ate host and are found worldwide. The definitive hosts include many avian species as
well as mammalian species. Some schistosomes will infect both avian and mammalian
species and others are more restricted. For example, the genus Allobilharzia has been
434 Pilny & Reavill

Fig. 3. Scarlet macaw (Ara macao) cerebellum with a cross-section through a Baylisascaris
species. This parasite is within the white matter and is supporting bilateral alae, a thin
eosinophilic cuticle, and a pseudocoelomic body cavity lined by a low musculature (hema-
toxylin-eosin stain). (Courtesy of D. R. Reavill, DVM, DABVP (Avian and Reptile & Amphibian
Practice), DACVP, Salt Lake City, UT.)

isolated only from swans31 and Anserobilharzia isolated only from geese. Avian schis-
tosomes have been described in at least 10 orders of birds, most commonly Chara-
driiformes (gulls, terns, plovers) and Anseriformes (swans, geese, and ducks).
Gigantobilharzia huronensis is most commonly found in passerine birds, such as
red-winged blackbirds (Agelaius phoeniceus), grackles (Quiscalus spp.), and mourn-
ing doves (Zenaida macroura) that frequent freshwater habitats.32 Currently there
are 20 avian schistosome species representing at least 8 genera; Allobilharzia, Orni-
thobilharzia, Austrobilharzia, Macrobilharzia, Trichobilharzia, Dendritobilharzia, Anser-
obilharzia, and Gigantobilharzia.33 Morphologic classification of schistosomes has
proven difficult in both the primary and secondary hosts and further classification
may rely on molecular biology and phylogenetic analyses to fully understand
their life cycle.34 In humans, cercarial dermatitis is considered an important emerging
disease that is driving more research in the biology of these trematodes, particularly
Trichobilharzia. Trichobilharzia represents the largest genus within the family
Schistosomatidae.
Schistosomes are digenetic trematodes with a 2-host life cycle. They colonize
many families of snails as first intermediate hosts. Most schistosome species are
transmitted by the freshwater pulmonate snail families Physidae, Lymnaeidae,
and Planorbidae. The cercarial stage penetrates the epithelial surface of the defin-
itive host (mammalian and avian). They then spend their adult lives primarily within
the vasculature of their host. All the members of these blood flukes live as separate
males and females within the vascular system of their vertebrate definitive
hosts. Most known schistosomes have a fresh water-based life cycle. This is true
of all known mammalian schistosomes and most of the avian schistosomes.
However, there are genera that have life cycles based in marine environments
with marine snail hosts and definitive hosts primarily being Charadriiformes (gulls
and terns).35
 Re-emerging Diseases of Selected Avian Species 435

Most of the schistosomes penetrate mucosal and/or epithelial surfaces directly. The
parasite may continue to migrate to other tissues, although the precise path is not fully
described in many species. Based on their predilection site, Trichobilharzia spp. can
be divided in visceral and nasal species.35 Visceral species migrate through the
viscera and can be found in mesenteric, renal, cloacal, and portal blood vessels,
whereas nasal species also may display a neurotropic mode of migration.35 With nasal
schistosomes, the migration can involve blood vessels or peripheral nerves leading to
the spinal cord and brain of the host. Once they reach the preadult stage in the
meninges, they will start to feed on blood and then migrate via an intravascular route
back to the nasal cavity. In some duck species, Trichobilharzia live in veins of the nasal
mucosa where they mature and produce eggs. The miracidia hatch from the eggs
directly in the tissue and leave the host during drinking/feeding by the infected birds.36
For visceral routes, many of the Trichobilharzia species will migrate to the intestinal
portal veins where there may be a development of hyperplastic endophlebitis, which is
characterized by severe myointimal hyperplasia that often obliterates the vascular
lumen. From here, the schistosome eggs will migrate across the intestinal mu-
cosa.31,37–39 Associated lesions in some ducks can include portal fibroplasia in the
liver, nonviable schistosomes in the bile ducts, and viable adult schistosomes in the
portal veins.40 The main lesions of Trichobilharzia brantae infection in Atlantic Brant
geese (Branta bernicla hrota) included thrombosis of the caudal mesenteric veins
with adult schistosomes in serosal and mesenteric blood vessels. The eggs in the in-
testinal wall elicited a fibrinohemorrhagic colitis.41 For parasite life cycles involving the
digestive tract, fecal examination can identify the trematode eggs.34
The clinical signs for trematode species migrating to the central nervous system
include behavioral changes, disorientation, paralysis, and death in some hosts.42
For species with intestinal vasculature migration, the vascular lesions may
contribute to emaciation and death by obstruction of venous return in the intestinal
and portal veins.38 The pathogenicity of the infection depends on many factors,
such as parasite load, duration of infection, and preferred site of the adult trematode.
The host inflammatory reactions are more significant with the immature schistosomes
(dermatitis) and the eggs (usually a granulomatous inflammatory reaction).35
An unexpected natural schistosome infection was described in a pet 8-month-old
female Nanday conure (Aratinga nenday). She presented for weight loss and
blood-flecked diarrhea before death. A fecal examination found eggs (large 83–
134  65–78 mm) containing a miracidium. The smooth shell supported the character-
istic small terminal spine or knob. On histologic evaluation, the colon and cloaca had
variable epithelial hyperplasia, masses of parasitic eggs, and severe chronic inflam-
mation. Trematode eggs were present in the lungs, liver, and kidney associated
with granulomas.43
Treatment of the infection in the final avian host has been studied in an attempt to
reduce the parasite load and attempt to control swimmer’s itch (cercarial dermatitis).
High doses (200 mg/kg IM) of praziquantel reduced the parasite load in common mer-
gansers44 and 1 oral dose of 34 mg/bird was effective in reducing the parasites in
mallards.45

Orthoreovirus
Avian orthoreoviruses belong to the family Reoviridae, genus Orthoreovirus. They
infect wild and farm-raised birds and are important fowl pathogens associated with
various syndromes, such as gastrointestinal malabsorption syndrome, tenosyno-
vitis/arthritis, delayed growth, and sudden death. They have also been isolated from
asymptomatic birds.
436 Pilny & Reavill

Scientists at the National Wildlife Health Center (NWHC), USGS, Madison, WI, have
identified reovirus as the cause of death in American Crows at several locations from
east to west across the United States, beginning in 2000. In January and February
2004, American Crows were found dead at the Pittock Conservation Area in Wood-
stock in southwestern Ontario.46 Hemorrhage and inflammation of the intestines
was the most common abnormality noted, and often was accompanied by inflamma-
tion and necrosis in the spleen. In 2008, an aggressive avian virus killed thousands of
crows across New York state over several weeks, according to an investigation by the
state Department of Environmental Conservation alerting its significance and linking it
to reovirosis. A case report of a wild hooded crow also diagnosed with the virus was
seen in Finland.47
Epizootic mortalities in American Crows (Corvus brachyrhynchos) during the winter
months have been recorded in North America for almost 20 years with common post-
mortem findings, including necrotizing enteritis, fibrinous splenic necrosis, and colitis.
These findings are consistent with infection with a Reovirus sp. Reovirosis shows a
clear seasonal presentation with cases occurring almost exclusively in winter months.
Data from 2016 to 2017 showed that reovirosis caused up to 70% of all recorded crow
deaths during winter months.48 Crows with positive orthoreovirus isolation from the
spleen or intestine were 32 times more likely to die with characteristic histologic
lesions of enteritis or enterocolitis and splenic necrosis than crows with negative isola-
tion results. A new study suggested that a novel orthoreovirus was the cause of winter
mortality (or reovirosis) of American Crows and placed the New York isolates in the
genus of Corvid orthoreovirus.

RENAL TREMATODES

Several trematode genera of the families Eucotylidae (genera Paratanaisia and Tanai-
sia) and Renicolidae (genera Renicola) have been identified within the upper urinary
tract of a variety of avian species.49
The digenetic trematode genus Paratanasia are known parasites of the urinary tract
of neotropical birds and have been identified in other regions of the world. The genus
consists of 3 species: Paratanaisia bragai, P robusta, and P confusa. These have a het-
eroxenous cycle with gastropod mollusks acting as the intermediate hosts. These
trematodes do not seem to be host-specific and have been identified in many species
of birds. Most intermediate hosts are land snails. The birds acquire the infection when
feeding on the mollusks affected with the metacercariae, the infective form. The adult
trematodes are found developing in the ureters, collecting ducts, and renal tubules of
the kidney. The birds reported as having this genus of trematodes parasitizing the kid-
neys include: several species of Columbiformes, Galliformes, many Passeriformes,
Psittaciformes,50,51 Strigiformes, Cuculiformes, Tinamiformes, and Ciconiiformes.52,53
Renicolids are trematodes that inhabit the renal tubules and ureters of molluscivo-
rous and piscivorous birds. The Manx shearwater (Puffinus puffinus), a migratory
seabird, and the king penguin (Aptenodytes patagonicus) have been identified as
the definitive hosts of Renicola sloanei. Only mild renal lesions were noted in a case
report of 2 dead Manx shearwaters. Macroscopically, small black multifocal areas
in the kidney were noted containing pairs of trematodes inside cyst-like structures
and microscopic findings were dilation of the collecting ducts associated with accu-
mulation of paired renicolids in the dilated ducts.54 Many other penguin groups and
several terns have been identified as supporting renal Renicola, although the species
was not determined. Clinically the infections were not interpreted as causing any sig-
nificant disease.55
 Re-emerging Diseases of Selected Avian Species 437

The basic life cycle consists of the excreted embryonated eggs from the host that
passively infect a mollusk. After the miracidium hatches, 2 generations of sporocysts,
cercariae, and metacercariae develop within the snail. The definitive host acquires the
infection by eating the parasitized mollusk.
In general, infected birds may have few if any clinical signs. Clinical signs noted have
included poor body condition, hypothermia, inactivity, and in some cases other con-
current infections. In species considered the usual definitive hosts, the infections are
considered incidental. In accidental hosts, infections with P bragai and P robusta may
result in death in a variety of psittacines (South American to Australian), white-eared
pheasants (Crossoptilon crossoptilon), and red bird-of-paradise (Paradisaea
rubra).50–52,56
On gross evaluation, there may be no significant lesions noted to enlarged kidneys
with a nodular appearance and urate stasis. With histology, these trematodes may be
identified with dilated cystic spaces of the distended ureters, collecting ducts, and tu-
bules. The adjacent renal parenchyma is generally compressed, and there may be a
variable amount of inflammation, primarily lymphocytic and in some cases heterophilic
with macrophages and other degenerative changes. The tubular lining cells are typi-
cally flattened and there may be interstitial fibrosis. Occasionally, eggs of this trema-
tode can be noted within the interstitial tissue, and these typically elicit more
significant inflammation.53 It seems that the primary inflammation is usually directed
against the eggs as opposed to the adult trematodes. The adult trematodes may
also be associated with some variable hyperplasia of the renal tubular epithelium
(Fig. 4). This is suspected due to the irritation of the lining epithelium by the integument
of the trematodes.
Diagnosis of this infection has primarily been on necropsy. From a search of the liter-
ature, there are no reports of antemortem diagnosis, such as identifying the trematode
eggs within the urine or urates. Once this trematode infection has been identified with
histology, controlling access to the intermediate host is the best form of control.

Fig. 4. Brown pelican (Pelecanus occidentalis) kidney with intraureter trematodes (T),
possibly Paratanasia confusa-based morphologically on the spines (arrows). There is exten-
sive epithelial hyperplasia (E) of the ureter (hematoxylin-eosin stain). (Courtesy of D. R.
Reavill, DVM, DABVP (Avian and Reptile & Amphibian Practice), DACVP, Salt Lake City, UT.)
438 Pilny & Reavill

Prophylactic treatment of praziquantel has been used in collections/aviaries.56 With

birds in conservation programs, eliminating or preventing infections is important
when considering release of infected/exposed birds and exposing naive populations
to the trematodes, especially in areas supporting appropriate intermediate hosts.

DISCLOSURE

The authors have nothing to disclose.

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